The heart is the center of a person's circulatory system. It includes an electro-mechanical system performing two major pumping functions. The left portions of the heart draw oxygenated blood from the lungs and pump it to the organs of the body to provide the organs with their metabolic needs for oxygen. The right portions of the heart draw deoxygenated blood from the body organs and pump it to the lungs where the blood gets oxygenated. These pumping functions are accomplished by cyclic contractions of the myocardium (heart muscles). In a normal heart, the sinoatrial node generates electrical impulses, called action potentials, at a normal sinus rate. The electrical impulses propagate through an electrical conduction system to various regions of the heart to excite the myocardial tissues of these regions. Coordinated delays in the propagations of the action potentials in a normal electrical conduction system cause the various portions of the heart to contract in synchrony to result in efficient pumping functions indicated by a normal hemodynamic performance. A blocked or otherwise abnormal electrical conduction and/or deteriorated myocardial tissue cause dyssynchronous contraction of the heart, resulting in poor hemodynamic performance including a diminished blood supply to the heart and the rest of the body. The condition where the heart fails to pump enough blood to meet the body's metabolic needs is known as heart failure.
Myocardial infarction (MI) is the necrosis of portions of the myocardial tissue resulted from cardiac ischemia, a condition in which the myocardium is deprived of adequate oxygen and metabolite removal due to an interruption in blood supply caused by an occlusion of a blood vessel such as a coronary artery. The necrotic tissue, known as infarcted tissue, loses the contractile properties of the normal, healthy myocardial tissue. Consequently, the overall contractility of the myocardium is weakened, resulting in an impaired hemodynamic performance. Following an MI, cardiac remodeling starts with expansion of the region of infarcted tissue and progresses to a chronic, global expansion in the size and change in the shape of the entire left ventricle. The consequences include a further impaired hemodynamic performance and a significantly increased risk of developing heart failure, as well as a risk of suffering recurrent MI.
Cardiac stimulation therapies have been applied to restore functions of the electrical conduction system and reduce the deterioration of myocardial tissue by delivering electrical pulses to the heart. Their potential benefits to a patient are achieved or maximized when such therapies are adaptive to the patient's cardiac condition and other physiological factors influencing the hemodynamic performance, which change over time. A cardiac stimulation therapy may also have unintended effects on the hemodynamic performance or cardiac remodeling, with the degree of impact dependent on the patient's cardiac condition and metabolic need. In one example, transiently delivering pacing pulses at a relatively high rate may provide a level of hemodynamic performance that satisfies the patient's instantaneous metabolic need for participating in an intense physical activity. However, delivering pacing pulses at a relatively high rate on a chronic basis may result in further deterioration of myocardial tissue. In another example, a cardiac stimulation therapy preventing further deterioration of myocardial tissue may significantly limit the patient's exercise capacity because the hemodynamic performance is further impaired when therapy is being delivered.
For these and other reasons, there is a need to modulate the delivery of cardiac stimulation therapies based on the patient's cardiac conditions and/or other physiological factors influencing the hemodynamic performance.